This presentation is made by Dr Ashok Jaisingani for study purpose, if any one like this than please give comment.

1. Dr Ashok Jaisingani

2.  Shock is the most common and important
cause of the death among the surgical
patients
 Death occurs rapidly as result of the
1- Profound state of the shock
2- Consequence of the organ ischemia
3- Reperfusion injury

3.  Shock is the systemic state of the low tissue
perfusion, which is inadequate for the
normal cellular respiration.
 With insufficient delivery of the oxygen and
glucose cells switch from aerobic to
inaerobic metabolism.

4.  Pathophysiology of the shock is divided in to
three categories
1- Cellular
2- Microvascular
3- Systemic

5.  Reduced tissues perfusion  dec. cellular
O2  switch from aerobic to anaerobic
metabolism  accumulation of the lactic
acid in the blood  “Systemic Metabolic
Acidosis”.
 As glucose within cells exhausted  stop
respiration  failure of Na+/K+ pump of
cellular membranes  lysosomal enzymes
become released  lyses of the cells
 Potassium released into the blood stream.

6.  As tissues ischemia progress  change in
the internal environment of the body 
activation of the immune and coagulation
systems.
 Hypoxia and acidosis activate
compliment and the prime neutrophils 
generation of the O2 free radicals and
release of the cytokines.
 Above two mechanism leads to injury to
endothelials cells of the capillaries 
damage endothelial cells become leaky 
tissues edema  exacerbating tissues
hypoxia

7.  Systemic pathophysiology involves
1- Cardiovascular system
2- Respiratory system
3- Renal System
4- Endocrine System

8.  Due to tissues edema  pre-load & after –
load decrease  Compensatory baro
receptor response  increase sympathetic
activity  release of the catecholamine 
tachycardia and systemic vasoconstriction
 Above mechanism not associated with the
shock result from the sepsis.

9.  Metabolic acidosis and increase sympathetic
response  increase respiratory rate and
minuet ventilation  increase the excretion
of the CO2  Compensatory respiratory
alkalosis.

10.  Due to dec. preload and afterload  dec.
perfusion pressure in the kidneys  reduce
filtration at glomerulus  dec. urine output
 activation of renin – angiotensin –
aldosterone system  further vasoconstri –
-on  increase water and sodium
reabsorbtion from kidneys  further edema
 exacerbating further ischemia.

11.  In addition to adrenal and renin-angiotensin
system, vasopressin release from the
hypothalamus in response to decrease
preload  vasoconstriction and reabsorbtion
of the sodium and water

12.  During period of the systemic hypoperfusion 
cellular and organ damage progress just because
of the direct effects of tissues hypoxia and local
activation of the inflammation.
 Further injury is also occurs once restoration of
the normal circulation  acid and K+ load that
has build up  myocardial depression, vascular
dilatation and hypotension.
 The cellular and humoral elements activated by
the hypoxia flushed back into circulation 
further endothelial injury  Acute lung injury,
acute renal injury, multiple organs failure and
death.
 Reperfusion injury only attenuated by reducing
extent and duration of the tissue hypoxia.

13.  Clinically shock is divided on the basis of the
initiating mechanism
1- Hypovolemic Shock
2- Cardiogenic Shock
3- Obstructive Shock
4- Distributive Shock
5- Endocrine Shock

14.  Hypovolemic shock is caused by the reduce
circulating volume. It may be due to following
causes
1- Hemorrhage
2- Non – Hemorrhagic
 Non-hemorrhagic causes includes following
1- Poor Fluid intake (dehydration)
2- Excessive loss of fluid in vomiting, diarrhea,
urinary loss as in diabetes and “third spacing” in
which fluid loss in GIT & interstitial space E.g.
bowl obstruction and pancreatitis.
 Hopovolaemia is most common cause of the
shock and in some degree also component of the
all other shock.

15.  Cardiogenic shock result from primary failure of the heart
to pump the blood to the tissues and causes of that shock
include followings
1- Myocardial Infarction
2- Cardiac Dysrhthemia
3- Valvular Heart Disease
4- Blunt myocardial Injury
5- Cardiomyopathy
 Cardiac insufficiency may also be caused by myocardial
depression resulting from
1- Endogenous factors (Bacterial and humoral agents as in
sepsis)
2- Exogenous factors (pharmaceutical and drug abuse)
 Evidence of the systemic hypertension with pulmonary or
systemic edema may co – exist with the classic signs of the
shock.

16.  There is reduction in preload because of
the mechanical obstruction of the cardiac
filling.
 Common causes of the obstructive causes
are followings
1- Cardiac Temponade
2- Tension Pneumothorax
3- Massive Pulmonary Embolus
 In each of the above situation there is
dec. filling of the left or right ventricles
leading to reduce preload  Fall In
Cardiac Output.

17.  That describe the cardiovascular response
in variety of the conditions such as
1- Septic Shock
2- Anaphylaxis
3- Spinal Cord Injury
 Inadequate organs perfusion accompanied
by the
1- Vascular dilatation
2- Hypotension
3- Low systemic vascular resistance
4- Inadequate afterload

18.  There is vasodilatation is caused by the
release of the histamine in the systemic
circulation.
 That occurs mostly in allergic reaction.

19.  In high spinal cord injury there is failure of
the sympathetic outflow and that leads to
inadequate vascular tone.

20.  There is release of the bacterial products
such as endotoxin and activation of the
cellular and humoral components of
immune system.
 There is maldistribution of blood flow at
microvascular level with arteriovenous
shunting and dysfunction of cellular
utilization of the oxygen.
 Mostly in the late phase of the septic
shock hypovolaemia result from fluid loss
into interstitial space and there may be
myocardial depression which complicate
the clinical picture.

21.  Endocrine shock may present as complication
of
1- Hypovolemic Shock
2- Cardiogenic Shock
3- Distributive Shock
 Causes Of Endocrine Shock
1- Hypo or Hyperthyroidism
2- Adrenal Insufficiency